Cardiac atria contain a family of peptides, collectively termed atrial natriuretic peptides (ANPs), which are derived from a common precursor and possess intrinsic natriuretic, diuretic, vasorelaxant and endocrine modulatory effects. Furthermore, recent immunocytochemical and radioimmunoassay (RIA) distribution studies have localized ANPs to areas of the CNS that suggest the ANPs are involved in central cardiovascular regulatory events and in the release and/or synthesis of certain pituitary gland hormones. Additional support for the possible involvement of ANPs in regulating pituitary gland function was obtained with the demonstration that high-affinity, specific ANP binding sites are present on pituitary gland membranes. Characterization by reversed phase high-pressure liquid chromatography and quantification by RIA of rat plasma ANPs revealed the presence of at least two forms of ANP ranging from 24-28 amino acids. Additional studies revealed that volume loading or pressor agents (e.g. adrenaline, vasopressin) which cause atrial stretch result in a rapid increase in circulating ANPs. The acute administration of ethanol to rats in order to achieve blood ethanol levels in the range of .2-.25% did not alter plasma levels of ANPs; however, chronic exposure of rats to ethanol vapors for 7-14 days lowered plasma ANP levels. On the basis of results obtained in vitro from cultured adult rat atrial cardiocytes, it would appear that our observed enhancement of ANPs in vivo are indirectly mediated since a number of pressor agents did not alter ANP secretion in vitro. To date only drugs or experimental conditions which alter intracellular Ca++ levels appear to modulate ANP secretion in cultured atrial myocytes.